Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 37, Issue 6, Pages 2098-2111Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X16661201
Keywords
C-type lectin; ischemia; middle cerebral artery occlusion; microglia; sterile inflammation
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Funding
- Australian National Health & Medical Research Council [1057846, 1060538]
- Spinal Cure Australia (Career Development Fellowship)
- Singapore National Medical Research Council Collaborative Research Grant [NMRC-CBRG-0102/2016]
- State Government of Victoria
- Australian Government
- University of Queensland
- Australian Research Council
- National Health and Medical Research Council of Australia [1057846, 1060538] Funding Source: NHMRC
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The C-type lectin Mincle is implicated in innate immune responses to sterile inflammation, but its contribution to associated pathologies is not well understood. Herein, we show that Mincle exacerbates neuronal loss following ischemic but not traumatic spinal cord injury. Loss of Mincle was beneficial in a model of transient middle cerebral artery occlusion but did not alter outcomes following heart or gut ischemia. High functional scores in Mincle KO animals using the focal cerebral ischemia model were accompanied by reduced lesion size, fewer infiltrating leukocytes and less neutrophil-derived cytokine production than isogenic controls. Bone marrow chimera experiments revealed that the presence of Mincle in the central nervous system, rather than recruited immune cells, was the critical regulator of a poor outcome following transient middle cerebral artery occlusion. There was no evidence for a direct role for Mincle in microglia or neural activation, but expression in a subset of macrophages resident in the perivascular niche provided new clues on Mincle's role in ischemic stroke.
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